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자료유형
학술저널
저자정보
Ko, Moon-Jeong (National Institution of Food and Drug Safety Evaluation, Korea Food and Drug Administration) Ahn, Joon-Ik (National Institution of Food and Drug Safety Evaluation, Korea Food and Drug Administration) Shin, Hee-Jung (National Institution of Food and Drug Safety Evaluation, Korea Food and Drug Administration) Kim, Hye-Soo (National Institution of Food and Drug Safety Evaluation, Korea Food and Drug Administration) Chung, Hye-Joo (National Institution of Food and Drug Safety Evaluation, Korea Food and Drug Administration) Jeong, Ho-Sang (National Institution of Food and Drug Safety Evaluation, Korea Food and Drug Administration)
저널정보
한국유전체학회 Genomics & informatics Genomics & informatics 제8권 제1호
발행연도
2010.1
수록면
41 - 49 (9page)

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Statins are competitive inhibitors of hydroxy-3-methyl glutaryl coenzyme A (HMG-CoA) reductase and used most frequently to reduce plasma cholesterol levels and to decrease cardiovascular events. However, statins also have been reported to have undesirable side effects such as myotoxicity and hepatotoxicity associated with their intrinsic efficacy mechanisms. Clinical studies recurrently reported that statin therapy elevated the level of liver enzymes such as ALT and AST in patients suggesting possible liver toxicity due to statins. This observation has been drawn great attention since statins are the most prescribed drugs and statin-therapy was extended to a larger number of high-risk patients. Here we employed rat primary hepatocytes and microarray technique to understand underlying mechanism responsible for statin-induced liver toxicity on cell level. We isolated genes whose expressions were commonly modulated by statin treatments and examined their biological functions. It is of interest that those genes have function related to response to stress in particular immunity and defense in cells. Our study provided the basic information on cellular mechanism of statin-induced cytotoxicity and may serve for finding indicator genes of statin -induced toxicity in rat primary hepatocytes.

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